The work presented in this thesis has explored the hypotheses that disturbances of insulin and of endogenous fibrinolysis are a feature of patients with established ischaemic heart disease and investigated the potential manipulation of these by an inhibitor of the angiotensin converting enzyme. The possibility that the presence of either a previous myocardial infarction or of heart failure might influence the development of hyperinsulinaemia was studied. Only patients with heart failure showed fasting hyperinsulinaemia, whereas the increased insulin response to an oral glucose load in those with heart failure or previous myocardial infarction was similar, and greater than the response in patients with stable angina. Hyperinsulinaemia has been previously associated with impaired peripheral muscle glucose uptake and metabolism and might contribute to the development of muscular fatigue on exertion in patients with previous myocardial infarction or with heart failure. Amongst patients with ischaemic heart disease who had a normal fasting plasma glucose, one fifth had impaired glucose tolerance on formal testing and this group exhibited significantly greater fasting and stimulated hyperinsulinaemia. Including all patients, there was an inverse relationship between left ventricular ejection fraction and fasting plasma insulin concentration. Impaired endogenous fibrinolysis has been associated with an adverse prognosis in patients with ischaemic heart disease. The effect of captopril upon tissue-type plasminogen activator and on plasminogen activator inhibitor type 1 was investigated in patients with recent uncomplicated myocardial infarction. Captopril caused a significant reduction in antigen levels of both type plasminogen activator and on plasminogen activator inhibitor type 1. This may help to explain the reduction in acute coronary syndromes that has been associated with the use of captopril following acute myocardial infarction.